Final answer:
The statement is true; short telomeres, rather than the absence of telomerase, explain cellular aging and related outcomes. Telomerase can rebuild telomeres, which is significant for aging research.
Step-by-step explanation:
The statement that it is short telomeres, not the absence of telomerase, that explains outcomes is true. Telomeres, which are the protective caps at the ends of chromosomes, naturally shorten each time a cell divides.
In most somatic cells, telomerase, an enzyme that can rebuild and lengthen telomeres, is not active. Consequently, as telomeres get progressively shorter, the cells age and eventually stop dividing. This telomere shortening is directly associated with aging, as well as an increased risk of age-related diseases.
The study of telomerase and its potential to lengthen telomeres is significant for its implications in regenerative medicine, particularly in the treatment of age-related conditions and diseases.